Open AccessMicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice
Author(s) -
Stefanie G. Wohl,
Marcus Hooper,
Thomas A. Reh
Publication year - 2019
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.179556
Subject(s) - biology , microrna , muller glia , phenotype , regeneration (biology) , microbiology and biotechnology , gene expression , gene , progenitor cell , regulation of gene expression , stem cell , genetics
Müller glial cells (MG) generate retinal progenitor (RPC)-like cells after injury in non-mammalian species, though this does not occur in the mammalian retina. Studies have profiled gene expression in these cells to define genes that may be relevant to their differences in neurogenic potential. However, less is known about differences in micro-RNA (miRNA) expression. In this study, we compared miRNAs from RPCs and MG to identify miRNAs more highly expressed in RPCs, and others more highly expressed in MG. To determine whether these miRNAs are relevant to the difference in neurogenic potential between these two cell types, we tested them in dissociated cultures of MG using either mimics or antagomiRs to increase or reduce expression, respectively. Among the miRNAs tested, miR-25 and miR-124 over-expression, or let-7 antagonism, induced Ascl1 expression and conversion of approximately 40% of mature MG into a neuronal/RPC phenotype. Our results suggest that the differences in miRNA expression between MG and RPCs contribute to their difference in neurogenic potential and that manipulations in miRNAs provide a new tool to reprogram MG for retinal regeneration.